http://www.cnr.it/ontology/cnr/individuo/prodotto/ID310062
Cigarette smoke alters IL-33 expression and release in airway epithelial cells (Articolo in rivista)
- Type
- Label
- Cigarette smoke alters IL-33 expression and release in airway epithelial cells (Articolo in rivista) (literal)
- Anno
- 2014-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.bbadis.2014.06.009 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Pace E.; Di Sano C.; Sciarrino S.; Scafidi V.; Ferraro M.; Chiappara G.; Siena L.; Gangemi S.; Vitulo P.; Giarratano A.; Gjomarkaj M. (literal)
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- Inst. of Biomedicine and Molecular Immunology (IBIM) - National Research Council (CNR), Palermo, Italy; School and Division of Allergy and Clinical Immunology, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy; Istituto Mediterraneo per i Trapianti e Terapie ad Alta Specializzazione (ISMETT), Palermo, Italy; Dipartimento di Anestesia, Rianimazione e delle'Emergenze - Università degli Studi di Palermo, Palermo, Italy (literal)
- Titolo
- Cigarette smoke alters IL-33 expression and release in airway epithelial cells (literal)
- Abstract
- Airway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored.Mini-BALs, but not sera, from smokers show reduced concentrations of IL-33. The expression of IL-33 was increased also in bronchial epithelium from smokers. 20% CSE reduced IL-33 release but increased the mRNA for IL-33 by real time PCR and the intracellular expression of IL-33 in bronchial epithelial cells as confirmed by flow cytometry, immunocytochemistry and western blot analysis. The effect of CSE on IL-33 expression was also observed in primary bronchial epithelial cells. IL-33 expression was mainly concentrated within the cytoplasm of the cells. LPS, an agonist of TLR4, reduced IL-33 expression, and an inhibitor of TLR4 increased the intracellular expression of IL-33. In conclusion, the release of IL-33 is tightly controlled and, in smokers, an altered activation of TLR4 may lead to an increased intracellular expression of IL-33 with a limited IL-33 release. © 2014 Elsevier B.V. (literal)
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